In the current year we examined the effect of glycocholate infusion on biliary dihydroxy bile acid secretion. Glycocholate initially fascilitated, and at high infusion rates close to its maximum biliary excretory capacity, inhibited dihydroxy bile acid excretion. In additional studies using theophylline, a non-bile salt dependent choleretic, and dehydrocholate, a non-micelle forming bile salt, we concluded that fascilitation of dihydroxy bile acid output by cholate infusion was related to displacement of the former bile acids from their hepatic storage sites by influx of cholate. Inhibition of dihydroxy bile acids output was related to competitive inhibition with cholate. In preliminary studies we determined that acute IV infusion of choline did not affect biliary lecithin excretion at high levels of cholate infusion. When choline was administered chronically via the gastrointestinal tract, however, biliary lecithin excretion increased at low cholate infusion rates, but it appeared that excretion remained limited at high cholate infusion rates. We will continue these studies in the forthcoming year to investigate mechanisms which limit biliary lecithin excretion at high cholate, as well as high chenodeoxycholate infusion levels.